However, to our knowledge, the present study is the first to elucidate that part of the mechanism whereby resistin positively enhances CRC cell adhesion to the endothelium is p53 tumor suppressor-independent and occurs through inducing canonical NF-κB activity to up-regulate the genes encoding the ICAM-1 and VCAM-1 adhesion proteins in HCT-116 cells. The gene discussed is RETN; the disease is colorectal carcinoma.